It is generally believed that allergic asthma and atopic diseases are induced as a variety of chemical mediators are released from the lung and other tissues to contract smooth muscles such as the bronchial muscle and pulmonary blood vessels or increase the permeability of blood vessels of the skin to thereby inflict various damages on various tissues.
Of such chemical mediators, histamine and SRS-A have been considered to be of the greatest significance. Recently, SRS-A was identified to be a mixture of leukotrienes LTC.sub.4, LTD.sub.4 and LTE.sub.4, which are peptides, and the multi-pronged physiological action of these leukotrienes (LT) and their association with various pathologic states have been extensively explored. By origin, SRS-A is a lipoxygenase-catalyzed metabolite of arachidonic acid and much interest has been focused on the role it plays as a substance involved in the onset or progression to refractoriness of bronchial asthma and other diseases arising from immediate type allergic reactions.
In fact, LTC.sub.4 and LTD.sub.4 strongly contract the isolated guinea pig and human tracheas and enhance the secretion of mucus from the human respiratory tract in vitro. Therefore, particular attention has been paid to their involvement in bronchial asthma.
Clinically, too, LT has been demonstrated in the sputum of patients with, for example, bronchitis in concentrations sufficient to produce physiological changes. It has also been reported that, in children with bronchial asthma, the blood LTC.sub.4 level is well correlated with the severity of the disease.
Asthma being set aside, it has been suggested that LT is associated with allergic rhinitis and dermatitis and even with ischemic diseases such as myocardial infraction etc., cardiac anaphylaxis, endotoxin shock, psoriasis and so forth.
Therefore, there is a mounting interest in the development of drugs which would either inhibit the production of SRS-A or antagonize SRS-A.
Thus, for example, FPL-55712, SKF-104353, WY-45911 and ONO-1078, among others, are known as LT antagonists. However, none have been commercially available as yet. [Tohn H. Musser et al., New development concerning Leukotriene Antagonists. Agents and Actions, 18 (3/4) 332 (1986), Drugs of the Future, 13(4) 317 (1988)].
Japanese Kokai Tokkyo Koho 62-198652 describes a group of compounds not alien to the compound of this invention, with the comment that some of the compounds have 5.alpha.-reductase inhibitory activity. The description in the claim of the corresponding specification might suggest that the compound of the present invention is subsumed therein but nowhere in the same specification is found a specific disclosure of any compound having a tetrazoyl group. Furthermore, there is no statement suggestive of the pharmacologic actions characteristic of the compound of the present invention. Incidentally, it has been proven that the compound of the present invention has no 5.alpha.-reductase activity at all.